ArticleJournal of neuro-oncology2010
Different molecular patterns in glioblastoma multiforme subtypes upon recurrence.
Article in Journal of neuro-oncology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 61 citations in OpenAlex.
- Prospective collection of tissue samples at autopsy in children with diffuse intrinsic pontine glioma.Cancer · 2010Trial
- Optimal clinicogenetic criteria for post-operative re-irradiation in recurrent glioblastoma: KROG 21-02.ESMO open · 2026Article
- Recurrent Glioblastoma-Molecular Underpinnings and Evolving Treatment Paradigms.International journal of molecular sciences · 2024Review
- Review
- EGFR Pathway Expression Persists in Recurrent Glioblastoma Independent of Amplification Status.Cancers · 2023Article
- Differences in stem cell marker and osteopontin expression in primary and recurrent glioblastoma.Cancer cell international · 2022Article
- Longitudinal Characteristics of Glioblastoma in Genome-Wide Studies.Pathology oncology research : POR · 2020Review
- Identification of potential crucial genes and molecular mechanisms in glioblastoma multiforme by bioinformatics analysis.Molecular medicine reports · 2020Article
- HJURP knockdown disrupts clonogenic capacity and increases radiation-induced cell death of glioblastoma cells.Cancer gene therapy · 2020Article
- Molecularly Targeted Agents in the Therapy of Pediatric Brain Tumors.Paediatric drugs · 2020Review
- Molecular Heterogeneity and Immunosuppressive Microenvironment in Glioblastoma.Frontiers in immunology · 2020Review
- Increased LGALS3 expression independently predicts shorter overall survival in patients with the proneural subtype of glioblastoma.Cancer medicine · 2019Article
- Whole-Genome Multi-omic Study of Survival in Patients with Glioblastoma Multiforme.G3 (Bethesda, Md.) · 2018Article
- Article
- The effects of 2-hydroxyglutarate on the tumorigenesis of gliomas.Contemporary oncology (Poznan, Poland) · 2018Review
- The Role of Class IA Phosphatidylinositol-4,5-Bisphosphate 3-Kinase Catalytic Subunits in Glioblastoma.Frontiers in oncology · 2017Review
- A comprehensive profile of recurrent glioblastoma.Oncogene · 2016Review
- Protein Analysis of Glioblastoma Primary and Posttreatment Pairs Suggests a Mesenchymal Shift at Recurrence.Journal of neuropathology and experimental neurology · 2016Article
- Targeted next generation sequencing of parotid gland cancer uncovers genetic heterogeneity.Oncotarget · 2015Article
- EGFR signaling and autophagy dependence for growth, survival, and therapy resistance.Cell cycle (Georgetown, Tex.) · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
One of the hallmarks of glioblastoma is its inherent tendency to recur. At this point patients with relapsed GBM show a survival time of only few months. The molecular basis of the recurrence process in GBM is still poorly understood. The aim of the present study was to investigate the genetic profile of relapsed GBM compared to their respective primary tumors. We have included 20 paired GBMs. In all tumor samples, we have analyzed p53 and PTEN status by sequencing analysis, EGFR amplification by semiquantitative PCR and a wide-genome fingerprinting was performed by microsatellite analysis. Among primary GBM, we observed twelve type 2 GBM, four type 1 GBM and four further GBM showing neither p53 mutations nor EGFR amplification (non-type 1-non-type 2 GBM). Upon recurrence, we have detected two molecular patterns of tumor progression: GBM initially showing either type 1 or type 2 profiles conserved them at the time of relapse. In contrast, non-type 1-non-type 2 GBM acquired the typical pattern of type 2 GBM and harbor EGFR amplification without p53 mutation. New PTEN mutations upon relapse were only detected in type 2 GBM. Additional LOH were more frequently identified in relapses of type 2 GBM than in those showing the type 1 signature. Taken together, our results strongly suggest that recurrences of GBM may display two distinct pattern of accumulation of molecular alterations depending on the profile of the original tumor.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.